Ethanol consumption induces apoptosis in a variety of tissues, among others in liver and lymphoid tissue.
Zinc has been shown to influence apoptosis of blood mononuclear cells by inhibiting the mitochondrial pathway of cell death. The aim of this study was to examine the influence of
zinc on spontaneous and in vitro alcohol-induced apoptosis of peripheral blood mononuclear cells (PBMCs) of patients with
alcoholic cirrhosis. PBMCs were isolated from the blood of 26 patients with
cirrhosis and 20 healthy controls. PBMCs and among them CD4+ T helper cells of cirrhotic patients exhibited accelerated spontaneous (without treatment) apoptosis in vitro. When apoptosis was induced in vitro by treating cells with 80 mM
ethanol, CD8+ T lymphocytes of a healthy control were more sensitive to
ethanol treatment than those of cirrhotic patients. Thirty micromolar
zinc supplementation inhibited both spontaneous and
ethanol-induced apoptosis of immune cells derived from the blood of the healthy control and cirrhotic patients. In sera of patients with
cirrhosis, an elevated level of
IL-12, but also sFas (CD95) and sFas
ligand (sFasL) was detected. Moreover, in vitro, PBMCs of cirrhotic patients spontaneously released more sFas and sFasL than control PBMCs.
Ethanol treatment significantly increased sFas, but decreased sFasL release from PBMCs of cirrhotic patients, while it only slightly affected control cells. As
zinc supplementation did not significantly influence sFas or sFasL release, it seems likely that it is rather the mitochondrial pathway of
ethanol-related immune cell death that may be inhibited by
zinc supplementation.